Beyond the Identification of Transcribed Sequences:
Functional, Evolutionary and Expression Analysis
12th International Workshop
October 25-28, 2002
Washington, DC


List of Abstracts * Speakers * Organizers * Authors * Original Announcement


Biological Roles for A to I Conversion in Untranslated Regions of mRNAs?

Daniel P. Morse1, P. Joseph Aruscavage2, Leath A. Tonkin2, Lisa Saccomanno2, Thomas Brodigan3, Michael Krause3, and Brenda L. Bass2
1Department of Chemistry, United States Naval Academy; 2Department of Biochemistry and Howard Hughes Medical Institute, University of Utah; 3Laboratory of Molecular Biology, NIDDK, NIH
Telephone: 410-293-6612
Fax: 410-293-2218
Email: morse@usna.edu

A family of RNA editing enzymes called adenosine deaminases that act on RNA (ADARs) convert adenosine to inosine within double-stranded regions of metazoan RNA.  Since inosine is read as guanosine by the translation machinery, editing in coding regions of mRNAs can result in codon changes.  Editing of this type in mammals results in the production of multiple, functionally distinct forms of a glutamate receptor subunit (GluR-B) and the serotonin 2C receptor. 

Using a largely unbiased search for inosine-containing mRNAs in C. elegans, we were surprised to find that most of the inosine occurred in untranslated regions or introns rather than in coding regions.  We wondered whether this was also true in mammals so, using the same method, we searched for ADAR substrates in human brain.  We identified 19 new human brain ADAR substrates, each of which was edited only in non-coding regions.  These results suggest that most inosine occurs in non-coding regions and that codon changes are the exception rather than the rule.

To further our understanding of ADAR function, we generated worms with deletions in one or both of the C. elegans ADAR genes.  The observed mutant phenotypes and the effect on RNA editing will be discussed.  More work will be required to determine whether alterations of editing in non-coding regions of specific ADAR substrates are responsible for the mutant phenotypes.



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